[热损伤大鼠组织肿瘤坏死因子-α（TNF-α）mRNA表达与肠道源性内毒素血症的关系]

[The relationship between tissue tumor necrosis factor-alpha(TNF-alpha) mRNA expression and gut-derived endotoxemia in rats after thermal injury].

作者信息

Zhai H, Yao Y, Lu L

机构信息

Burn Institute, 304th Hospital of People's Liberation Army, Beijing 100037.

出版信息

Zhonghua Zheng Xing Shao Shang Wai Ke Za Zhi. 1999 Nov;15(6):424-7.

PMID:11501076

Abstract

OBJECTIVE

To investigate the dynamic changes in tumor necrosis factor-alpha(TNF-alpha) mRNA expression and the relationship between TNF-alpha mRNA and gut-derived endotoxemia in rats after thermal injury.

METHODS

56 male Wistar rats were subjected to a 35% total body surface area full-thickness thermal injury and randomly divided into 3 groups: normal controls, 35% III* injury group, and polymyxin B treatment group. Plasma endotoxin was measured by limulus amebocyte lysate test, and tissue TNF-alpha mRNA expression was determined by reverse transcription polymerase chain reaction (RT-PCR).

RESULTS

It was found that a significant elevation of endotoxin concentration in both portal and systemic circulation was observed at 2 hours after thermal injury, peaking at 8 hours (P < 0.05-0.01) and lowering at 24 hours. Meanwhile, TNF-alpha mRNA expression significantly increased in liver, lung, intestine, and kidney at 2 hours, peaking at 8 hours, and a high level was maintained till 24 hours. However, treatment with a low-dose polymyxin B could lower both portal and systemic endotoxin levels, and markedly inhibit TNF-alpha mRNA expression in various organs. In addition, a positive correlation between portal endotoxin concentration and pulmonary, intestinal and renal TNF-alpha mRNA expression was noted (r = 0.365-0.484, all P < 0.05).

CONCLUSION

This study suggests that major burns can lead to a marked elevation of tissue TNF-alpha mRNA expression in vital organs, which may be associated with gut-derived endotoxemia caused by acute thermal injury.

摘要

目的

探讨热损伤大鼠肿瘤坏死因子-α（TNF-α）mRNA表达的动态变化及其与肠道源性内毒素血症的关系。

方法

将56只雄性Wistar大鼠造成35%总体表面积的全层热损伤，随机分为3组：正常对照组、35%Ⅲ度损伤组和多黏菌素B治疗组。采用鲎试剂法检测血浆内毒素，逆转录聚合酶链反应（RT-PCR）法测定组织TNF-α mRNA表达。

结果

热损伤后2小时门静脉和体循环内毒素浓度显著升高，8小时达峰值（P<0.05-0.01），24小时降低。同时，肝、肺、肠和肾组织中TNF-α mRNA表达在2小时显著增加，8小时达峰值，并维持在高水平直至24小时。然而，低剂量多黏菌素B治疗可降低门静脉和体循环内毒素水平，并显著抑制各器官TNF-α mRNA表达。此外，门静脉内毒素浓度与肺、肠和肾组织TNF-α mRNA表达呈正相关（r=0.365-0.484，均P<0.05）。